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At least 19 recordsLinked to original sources

Treatment of steatorrhoea in cystic fibrosis: a comparison of enteric-coated microspheres of pancreatin versus non-enteric-coated pancreatin and adjuvant cimetidine.

Enteric-coated microspheres of pancreatin were compared with non-enteric-coated pancreatin combined with cimetidine taken 40 min before meals in the treatment of patients with cystic fibrosis. Fourteen adults with steatorrhoea due to cystic fibrosis were investigated in an open, randomized crossover study, over two consecutive 28-day treatment periods. Lipase intake was adjusted to each patient's previous requirements and was the same during both months; they were instructed to continue with their normal diet. Patients collected faeces for 72 h at the end of each month and completed diary cards daily throughout. Bowel actions were less frequent on enteric-coated microspheres of pancreatin than on non-enteric-coated pancreatin/cimetidine (1.7 vs. 2.4/day; P less than 0.001) and stool character was improved (P less than 0.001). Mean daily faecal weight was similar on enteric-coated microspheres of pancreatin to that on the combination (254 g vs. 291 g; N.S.), whereas daily faecal fat excretion tended to be less on enteric-coated microspheres of pancreatin (21 g vs. 27 g; N.S.), and percentage fat absorption tended to be greater (81% vs. 73%; N.S.). Mean body weight increased by 0.3 kg on enteric-coated microspheres of pancreatin and fell by 0.1 kg on the combination (N.S.). These data indicate that enteric-coated microspheres of pancreatin are at least as effective as non-enteric-coated pancreatin with cimetidine in the treatment of steatorrhoea in cystic fibrosis.

Adult↗

Monitoring pancreatin supplementation in cystic fibrosis patients with the 13C-Hiolein breath test: evidence for normalized fat assimilation with high dose pancreatin therapy.

BACKGROUND: 13C-Hiolein is a randomly 13C-labeled mixture of long chain triglycerides synthesized by algae. METHODS: Because the 13C-Hiolein breath test is a suitable noninvasive tool to detect and monitor pancreatic steatorrhea, we used this new breath test for monitoring the effect of enzyme replacement therapy with an acid resistant enteric coated polydisperse pancreatin preparation (1.500 U/kg d) in children with cystic fibrosis. RESULTS: Administration of 1.5 mg/kg 13-C-Hiolein together with a physiological mixed meal (1.5 g/kg rice cookies, containing 25% fat and 37% starch) resulted in significantly higher breath 13CO2/12CO2 ratios in controls than in cystic fibrosis children (maximal delta over baseline responses (DOBmax) 39.2 +/- 18.1% vs. 13.1 +/-13.9%; p < 0.001). With pancreatin, DOBmax in the cystic fibrosis patients responses returned completely to normal (39.2 +/- 29.2% DOBmax). A breath hydrogen increase indicating the malassimilation of starch was noticed in one patient with severe pancreatic insufficiency only. CONCLUSION: In contrast to fecal fat analysis, the 13C-Hiolein breath test reflects postprandial fat assimilation immediately after a given, labeled meal. Monitoring the oxidative fate of physiological test meal with a stable isotope breath test, this study shows that fat assimilation in cystic fibrosis patients can be normalized with high dose pancreatin.

Adolescent↗

[A comparative cross-over study of pellet pancreatin and tablet pancreatin in chronic pancreatitis].

We have made a comparative cross study of 30 patients with chronic pancreatitis and steatorrhea. The aim of the study has been to compare the effectiveness of a new galenic form of pancreatin, in pellets, with the common galenic presentation, in tablets. In all the cases the cause of pancreatic failure was alcoholism. In both groups the treatment was administered during seven days, after a period of wash out. We evaluated steatorrhea and clinical symptoms, including the typical abdominal pain. (The doses administrated were 12 tablets/day or 9 pellets/day.) Statistically there was a significant decrease of steatorrhea p less than 0.01.

Abdominal Pain↗

[Effect of pancreatin on diabetes mellitus in chronic pancreatitis].

The effect of pancreatin on insulinopenic diabetes was studied in 10 patients with chronic pancreatitis and exocrine function impairment. All patients were treated for 4 days in a randomized crossover trial with either pancreatin (6 x 2 capsules, 6 x 300 mg/d) or placebo. Blood glucose levels were determined 7 times every day and night. On day 5, the patients were studied by a glucose sensor with adjustment of blood glucose to 120 mg/dl until 8.00 in the morning. A test meal was applied with 2 capsules pancreatin or placebo. Blood glucose and plasma levels of C-peptide, glucagon and pancreatic polypeptide (PP) were determined in regular intervals for 4 hours. Blood glucose levels were not significantly altered by pancreatin. As shown by M-value according to Schlichtkrull (21.6 +/- 2.9 versus 32.4 +/- 7.4), there was a tendency towards smaller oscillations of blood glucose with pancreatin treatment. C-peptide levels (basal 0.081 +/- 0.008 ng/ml; postprandial 0.119 +/- 0.013 ng/ml) were not significantly altered by the administration of pancreatin. Basal and postprandial glucagon and PP plasma levels were not influenced by pancreatin. From these results, we conclude that pancreatic enzyme supplementation does not significantly alter the requirement of insulin in patients with diabetes mellitus secondary to chronic pancreatitis. Possible disturbances of the enteroinsular axis are discussed in this paper.

Blood Glucose↗

Pancreatin enhanced erosion of and macromolecule release from 2,2-bis(2-oxazoline)-linked poly(epsilon-caprolactone).

The degradation and erosion of solvent cast films and injection molded bars prepared from poly(epsilon-caprolactone) (PCL) and 2,2'-bis(2-oxazoline) linked poly(epsilon-caprolactone) (PCL-O) were evaluated in simulated gastric fluid (SGF) (pH 1.2, pepsin present) and in simulated intestinal fluid (SIF) (pH 7.5, pancreatin present). After incubation of the polymer films (10 mg) and bars (70 mg) in the medium, the resulting decrease in molecular weight (degradation) was determined by size exclusion chromatography and the weight loss of the preparations was measured. In addition, the effect of pancreatin on FITC-dextran (MW 4400) release from PCL and PCL-O microparticles, prepared by w/o/w double emulsion technique, was studied. No degradation or weight loss was observed for either PCL or PCL-O films in SGF (12 h incubation, 37 degrees C). When compared to PBS pH 7.4, pancreatin hardly enhanced the weight loss of PCL films and bars. In contrast, pancreatin enhanced substantially erosion of PCL-O films and bars. Unlike PCL preparations, the PCL-O preparations showed surface erosion in SIF. Pancreatin increased considerably FITC-dextran release from both PCL and PCL-O microparticles. In conclusion, the present results demonstrate the enzyme sensitivity of the novel PCL-O polymer. In addition, the results show that pancreatin present in intestinal fluid may substantially affect drug release from PCL based preparations.

Macromolecular Substances↗

Pancreatin-EDTA treatment affects buoyancy of cells in Cohn fraction V protein density gradients without residual effect on cell size.

The buoyancy of suspension-grown Mastocytoma P815 X-2 cells in albumin-rich Cohn fraction V protein (CFVP) density gradients was found to be affected by prior incubation of the cells in pancreatin-EDTA salt solution. Whereas in pH 5.2 CFVP, pancreatin-EDTA treated cells behaved as if of reduced density when compared with the control 'undigested' group, in pH 7.3 CFVP they behaved as if of increased density. By contrast, pancreatin-EDTA treatment had no effect on the buoyancy of mastocytoma cells in polyvinylpyrrolidone-coated colloidal silica (PVP-CS, Percoll T.M.) density gradients of either pH 5.2 or pH 7.3. As cell size determinations failed to reveal alterations in cell size either as a direct result of pancreatin-EDTA treatment or as a combined consequence of such treatment and exposure to CFVP either with or without centrifugation, a mechanism involving a change in cell density other than during the centrifugation process itself seems unlikely. Binding studies employing 125I-CFVP, although indicating that CFVP bound to cells at 4 degrees, failed to reveal a pancreatin-EDTA treatment-related difference in the avidity of this binding. Although the mechanism of the pancreatin-EDTA-induced buoyancy shift in CFVP remains obscure, the absence of such an effect in PVP-CS suggests that the latter cell separation solution may more accurately be used to determine cell density.

Animals↗

[Dose-dependent effect of pancreatin replacement upon the pancreatic function in the period after pancreatic surgery].

AIMS: Disturbance of the exocrine function can persist for several weeks following pancreatic surgery. Active proteases in the duodenal lumen may help to recover exocrine function, but the effect can depend on dosage. METHODS: A placebo-controlled trial of enteric-coated pancreatin (Kreon 25,000 U lipase [A] and Kreon 10,000 U lipase [B]; 3 x 1 caps/day) was performed for 2 weeks following pancreatic surgery (resection or drainage operation in each group). A total of 60 patients were randomized, 20 to A and B pancreatin groups each, and 20 to the placebo group. We tested exocrine function via faecal elastase determinations, amylum tolerance test (ATT) and checks on the symptoms of maldigestion. RESULTS: After medication for 10 days, in group A there was evidence of the beneficial effect of pancreatin suggested by 35% improvement in ATT, unchanged body weight and disappearance of maldigestion. In group B, positive influence of pancreatin was confirmed only in those patients who underwent drainage operation, with moderate improvement of the symptoms of maldigestion and an almost unchanged body weight. In the control group and in resected patients in group B, abnormal ATT and maldigestion remained, while average body weight decreased by 3.5 kg. In all groups, no significant change was noted in the elastase concentration. CONCLUSION: The results suggest that dose-dependent enteric-coated pancreatin treatment after pancreatic surgery may lead to rapid improvement in the exocrine pancreatic function, probably by reducing the cholecystokinin response to food stimulation. This is an important indication for enteric-coated pancreatin medication.

Adult↗

A double-blind, randomized, multicentre, crossover study to prove equivalence of pancreatin minimicrospheres versus microspheres in exocrine pancreatic insufficiency.

BACKGROUND: Modern pancreatin preparations consist of enteric-coated microspheres to protect the enzymes from gastric acid. There are, however, no clinical trials comparing different sizes of pancreatin microspheres with regard to fat excretion and fat intake. AIM: To prove both equivalent efficacy and safety of conventional pancreatin microspheres and smaller pancreatin minimicrospheres in patients with exocrine insufficiency due to chronic pancreatitis. METHODS: In this prospective, randomized, double-blind, multicentre, crossover trial, patients with a stool fat excretion of > 7.5 g/day during a placebo period were randomly assigned either to the minimicrosphere/microsphere treatment sequence or vice versa. The primary end-point was the coefficient of fat absorption, which was calculated from fat excretion and fat intake during the course of a standardized diet. Stool weight, clinical symptoms and the safety of the preparations were also evaluated. RESULTS: Thirty-seven patients entered the study, of whom 23 fulfilled the criteria for the crossover period. In the per protocol analysis (n=18), the 90% confidence intervals for the coefficient of fat absorption of both crossover periods lay entirely within the equivalence range (P=0.02). The intention-to-treat analysis revealed similar results, but the equivalence range was slightly missed (P=0.07). Similar results were obtained for the secondary parameters and the reported adverse events. CONCLUSIONS: Pancreatin minimicrospheres have been shown to be equally effective as microspheres in improving the coefficient of fat absorption in patients with exocrine insufficiency due to chronic pancreatitis.

Adult↗

In vitro biodegradation of polyhydroxybutyrate-hydroxyvalerate microcapsules exposed to Hank's buffer, newborn calf serum, pancreatin and synthetic gastric juice.

Spherical microporous reservoir-type microcapsules, fabricated using a W/O/W double emulsion technique with solvent evaporation and composed of 330 kD poly(beta-hydroxybutyrate-hydroxyvalerate (P(HB-HV)) (10.8% HV)/20% PCL II containing a range of bovine serum albumin (BSA) loadings, were incubated in Hank's buffer, pH 7.4, newborn calf serum (NCS), 1.5% pancreatin and synthetic gastric juice containing 10% pepsin over 30 days, and their percentage weight loss (PWL) and change in ultrastructural morphology monitored by gravimetry and stereoscan electron microscopy (SEM), respectively. The greatest percentage weight loss from microcapsules was observed after incubation in NCS and decreased in the other NCS > pancreatin > synthetic gastric juice > Hank's buffer. Only 5, 10 and 15% bovine serum albumin (BSA) loaded microcapsules incubated in Hank's buffer and synthetic gastric juice showed a significant increase in PWL with increasing percentage BSA loading. The overall sequence of changes in structural morphology due to biodegradation occurred at different rates in the different 'physiological' media. An initial increase in micropore diameter was followed by the coalescence of microspores to form macroporous pits (Hank's buffer). Further biodegradation in NCS, pancreatin and synthetic juice was characterized by significant surface and bulk erosion. Only in pancreatin and NCS did biodegradation proceed to a loss of spherical shape and partial (pancreatin) and almost total (NCS) disruption of microcapsule structure after 30 days.

Animals↗

Treatment of pancreatic exocrine insufficiency after pancreatic resection. Results of a randomized, double-blind, placebo-controlled, crossover study of high vs standard dose pancreatin.

BACKGROUND: Steatorrhea following major pancreatic resection can be difficult to control, requiring high doses of pancreatic enzyme supplements. The aim of this study was to demonstrate equivalent efficacy of high-dose and standard-dose pancreatin in treating steatorrhea after pancreatectomy. METHODS: A randomized, double-blind, crossover study was conducted with a 2-wk run-in period for stabilization on a suitable dose of standard-dose pancreatin and two 14-d treatment periods using either high-dose or standard-dose pancreatin at this dosage. Parameters used to demonstrate efficacy of treatment were stool fat excretion, stool volume, and clinical symptoms. RESULTS: Thirty-nine patients who had undergone total or partial pancreatectomy were randomised; 37 completed all parts of the study. During stabilization, the mean daily capsule intake was 19.4 (range 9-54); even so, 22 (56%) patients had stool fat excretion > 7 g/d. There were significant correlations between stool fat excretion and stool volume (p < 0.0001) and stool frequency (p < 0.01), but not with indices of abdominal pain and global symptoms. Both high-dose and standard-dose pancreatin demonstrated statistically similar efficacy in the treatment period. CONCLUSION: The use of high-dose pancreatin for the treatment of pancreatic insufficiency in patients following pancreatectomy should significantly reduce capsule intake with increased convenience and greater compliance rate. Our results, however, indicate that further progress is needed to resolve steatorrhea following pancreatic resection.

Adult↗

[Effect of pancreatin replacement on pancreatic function in the postoperative period after pancreatic surgery].

There is evidence that disturbances of exocrine function can persist for several weeks following pancreatic surgery. Active proteases in the duodenal lumen may help to recovery of exocrine function. A placebo-controlled trial of enteric-coated pancreatin (25,000 U lipase; 3 x 1 caps/day) was performed during 2 weeks following pancreatic surgery (resection and drainage operation). A total of 39 patients were randomized, 20 to pancreatin group and 19 to placebo group. The exocrine function was tested via serum and faecal elastase determinations, the amylum tolerance test (ATT) and checks on the symptoms of maldigestion. After medication for 10 days, there was evidence of the beneficial effect of pancreatin suggested by a 35% improvement in ATT, an unchanged body weight and the disappearance of symptoms of maldigestion. In the control group, abnormal ATT and symptoms of maldigestion were remained, while the body weight decreased with by 3.5 kg. In both groups, no significant change was noted in the elastase concentration. The results suggest that enteric-coated pancreatin treatment after pancreatic surgery may lead to a rapid improvement of exocrine pancreatic function, probably by reducing the cholelcystokinin response to stimulation by food and represent a new indication of the enteric-coated pancreatin medication.

Chronic Disease↗

A new method of testing pancreatin therapy in vivo by the use of a peroral chymotrypsin substrate 4-(N-acetyl-L-tyrosyl)aminobenzoic acid.

The efficacy of pancreatin in vivo was determined in 14 patients with advanced pancreatic insufficiency using a peroral test with 2 g of chymotrypsin substrate, 4-(N-acetyl-L-tyrosyl)aminobenzoic acid, the Lundh test meal and 1000 ml tea. Chymotrypsin hydrolysis was quantified by 4-aminobenzoic acid excreted in 6-hr or 8-hr urine samples. After a control test without pancreatin, one or two tablets of Panpur (Nordmark-700 mg of pancreatin and 50 mg of bile per tablet) were applied simultaneously with the Lundh meal on repeated examinations. The urinary excretion of 4-aminobenzoic acid was restored to normal values in 5 subjects during both sampling periods. With this method, stimulated and substituted chymotrypsin is measured at the same time. The conditions of the tests, both with and without pancreatin replacement, are fully comparable and thus the significance of factors modifying the activity of enzymic components in the digestive tube is limited. The method appears appropriate for the institution of an effect pancreatin therapy and its control in vivo.

4-Aminobenzoic Acid↗

Effects of high-lipase pancreatin on fecal fat, neutral sterol, bile acid, and short-chain fatty acid excretion in patients with pancreatic insufficiency resulting from chronic pancreatitis.

CONCLUSIONS: Steatorrhea was almost completely stopped and malabsorption of neutral sterols and short-chain fatty acids was reduced by treatment of high-lipase pancreatin in Japanese patients with pancreatic insufficiency whose dietary fat consumption is low. METHODS: Fifteen patients with chronic pancreatitis complicated by steatorrhea who consumed an average of 48 g of dietary fats a day were selected as subjects and given 3 g of high-lipase pancreatin (lipase, 379,800 USP U/g), at each meal (total daily dose is 9 g) for a mean duration of 28.5 d. Fecal output and fecal fat neutral sterol, bile acid, and short-chain fatty acid excretion were determined before and after the course of pancreatin therapy. RESULTS: Pancreatin administration resulted in significant reductions (P < 0.01) in fecal output (from 243.2 to 149.1 g), excretion of fecal fat, (from 12.3 to 3.9 g), animal sterols (from 816.3 to 604.6 mg), and short-chain fatty acids (from 52.6 to 18.5 mM). In contrast, no marked changes were recorded in fecal excretion of beta-sitosterol (a plant sterol), bile acids, or the hydroxy fatty acid fraction. Fecal fat and short-chain fatty-acid excretion showed strong correlations with fecal output.

Adult↗

In vitro biodegradation of poly(beta-hydroxybutyrate-hydroxyvalerate) microspheres exposed to Hanks' buffer, newborn calf serum, pancreatin and synthetic gastric juice.

Spherical BSA loaded microporous matrix type microspheres composed of P(HB-HV) blended with 20% PCL II and fabricated using 0/W emulsification with solvent evaporation have been incubated in Hanks' buffer, pH 7.4; newborn calf serum; 1.5% pancreatin and synthetic gastric juice over 30 days and their percentage weight loss (PWL) and changes in ultrastructural morphology monitored by gravimetry and SEM respectively. The greatest percentage weight loss was observed after incubation in newborn calf serum and decreased in the order newborn calf serum > pancreatin > synthetic gastric juice > Hanks' buffer. Only incubation in synthetic gastric juice and Hanks' buffer produced a significant increase in PWL with increasing theoretical percentage loading. Incubation in Hanks' buffer produced limited surface erosion leading to an increase in micropore diameter and the coalescence of micropores to from surface pits. With pancreatin, surface erosion led to the disappearance of surface micropores and a reduction in microsphere diameter. Subsequent fracturing of the microsphere surface facilitated the breakup of the matrix. In synthetic gastric juice there was little surface erosion and surface flaking and bulk erosion were responsible for the breakup of the matrix. In newborn calf serum, spherical shape was maintained despite a reduction in microsphere diameter. Bulk erosion in the form of large macroporous pits extending deep into the matrix gave the microspheres a hollow appearance. The enhanced biodegradation in NCS and significant surface erosion in pancreatin was assumed to be due to the effects of exogenous enzyme activity in addition to simple ester hydrolysis.

3-Hydroxybutyric Acid↗

[Efficacy of a new microencapsulated pancreatin versus a conventional preparation, in the treatment of steatorrhea of pancreatic origin].

Malabsorption of pancreatic origin has been traditionally treated with pancreatic enzymes, but the effectiveness of treatment has been limited, related to the scant enzymatic activity of preparations, enzyme lability to acid attack and deficient mixing with the intestinal bolus, among other factors. We studied the efficacy of a new pancreatic enzyme preparation in the form of pellets, which mix easily with the intestinal bolus, are protected against gastric acid attack and have a high lipase concentration (Creon, Kalichemie-Pharma), as compared to traditional unprotected pancreatin in the form of tablets (Pankreon 700). The study was open, comparative and crossover, and included 12 patients. The diagnosis was chronic alcoholic pancreatitis in 10 cases and idiopathic pancreatitis in 2, with a steatorrhea of more than 10 g/24 h and a basal gastric pH less than 2.5. The duration of treatment was 3 weeks, using a diet containing 100 g of fat. The first week served as a control, and in the 2nd and 3rd treatment was given in the form of 7 capsules of Creon (2.1 g pancreatin and 70,000 UFIP lipase) or 17 tablets of Pankreon 700 (11.9 g pancreatin and 476,000 UFIP lipase) by randomized assignment. Our results confirm the beneficial effects observed by others. Steatorrhea was significantly reduced, up to 45.6% with Pankreon 700 and 57% with Creon, in spite of a dose that had 6.8 times less lipase activity, 5.6 times less pancreatin weight and 2.4 times fewer units ingested (capsules/tablets). Patients showed significant weight gain. At 30 days of treatment with Creon, steatorrhea had declined 70% and the weight gain was significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Plaque enhancement of enteroviruses by magnesium chloride, cysteine, and pancreatin.

Wallis, Craig (Baylor University College of Medicine, Houston, Tex.), Fred Morales, Joycelyn Powell, and Joseph L. Melnick. Plaque enhancement of enteroviruses by magnesium chloride, cysteine, and pancreatin. J. Bacteriol. 91:1932-1935. 1966.-Plaque formation of 21 echoviruses (types 1-6, 9, 13, 15-19, 23-26, 29-32) and 8 coxsackieviruses (B1-6, A7, and A9) was enhanced by increased concentrations of MgCl(2), l-cysteine, and pancreatin in agar overlay medium. In most cases, cationic and anionic polymers (diethylaminoethyl dextran, dextran sulfate, or protamine sulfate) were ineffective. All strains of poliovirus and group B coxsackieviruses were enhanced under agar by MgCl(2). Five of the eight coxsackieviruses tested were also enhanced by cysteine or pancreatin. Certain enteroviruses, which have been difficult to assay by plaque method, can now be quantified effectively by incorporation of additives such as MgCl(2), cysteine, or pancreatin into the overlay medium.

Chlorides↗

Pancreatin therapy in patients with insulin-treated diabetes mellitus and exocrine pancreatic insufficiency according to low fecal elastase 1 concentrations. Results of a prospective multi-centre trial.

BACKGROUND: Recently, high prevalence of exocrine dysfunction in diabetic populations has been reported. Patients with fecal elastase 1 concentration (FEC) <100 microg/g have also been demonstrated to suffer from steatorrhea in about 60% of cases, indicating the need of pancreatic enzyme replacement therapy. Until now, there have only been a few reports on the use of enzyme replacement therapy in diabetic patients with exocrine pancreatic insufficiency. This investigation was designed to evaluate the impact of enzyme-replacement therapy on glucose metabolism and diabetes treatment in a prospective study of insulin-treated patients with diabetes mellitus. METHODS: A total of 546 patients with diabetes mellitus requiring insulin treatment were screened for exocrine dysfunction by FEC measurements. One hundred and fifteen patients (21.1%) had FEC <100 microg/g (normal >200 microg/g). Of these, 95 patients entered the study and 80 patients were randomized to receive either pancreatin (Creon) (39 patients) or placebo (41 patients) in a double-blind manner. Parameters of glucose metabolism, diabetes therapy and clinical symptoms were recorded in standardized protocols for 16 weeks. RESULTS: During the observation phase of 16 weeks, there were no significant differences between both groups concerning HbA(1c), fasting glucose levels, 2-h pp glucose levels, clinical parameters and safety parameters. A reduction in mild and moderate hypoglycemia was observed in the pancreatin group at the end of the study. CONCLUSIONS: Pancreatin therapy can be used safely in patients with diabetes mellitus and exocrine dysfunction. Parameters of glucose metabolism were not improved by enzyme replacement therapy.

Diabetes Mellitus, Type 1↗